Oronasal Fistula with Palatal Involvement Secondary to Cocaine Use

Abstract

Vasoconstriction is a well-known local sympathetic effect of cocaine that may lead to ischemia, inflammation, ulceration and ultimately necrosis of the nasopharyngeal structures implicated by snorting cocaine. 2 Nasal septal perforation is present in 4.8% of abusers, making it the most common complication of cocaine abuse. 3 Chronic cocaine use may contribute to larger lesions and further destruction of the surrounding osteocartilaginous structures. Specifically, the destruction of nasal and midfacial bones and soft tissues can lead to a syndrome called cocaine-induced midline destructive lesion (CIMDL). The diagnosis of CIMDL requires at least 2 of the following clinical or radiologic findings: nasal septal perforation, lateral nasal wall destruction, and hard palate involvement. 4 We describe a patient with a history of cocaine abuse and signs of CIMDL, with midfacial destruction of the nasal septum and hard palate creating an oronasal fistula. To the best of our knowledge, we believe this is the first case of CIMDL with oronasal fistula reported in Canada. case presentation A 60-year-old male was referred to us with a 1-month history of a “hole” in his hard palate that caused fluids to leak out of his nose when drinking. Prior to presentation, he had been using denture adhesive gel as a temporizing measure for the palatal defect. He also disclosed that he had a nasal deformity, which previous physicians had attributed to his long history of cocaine snorting. The oral and nasal lesions were not associated with bleeding, pain, B-symptoms, nasal obstruction or recurrent sinusitis. His past medical history was notable for asthma and hypertension. His social history revealed a lifetime of tobacco use and many years of chronic cocaine use. On physical examination, the patient looked well and was in no acute distress. The nasal vestibules were intact bilaterally with no erosion of the columellar skin. Anterior rhinoscopy revealed complete loss of the cartilaginous nasal septum, without saddle nose deformity. Flexible nasopharyngoscopy showed extensive mucosal crusting, severe atrophy of the turbinates bilaterally but no polyps or suspicious growths. Examination of the oral cavity showed normal mucosa and dentition overall, with a single 1 cm perforation at the midline of the hard palate, communicating with the floor of the nasal cavity. The hard palate was quite soft in the area surrounding the perforation, suggesting bone loss of 2‐3 cm in circumference. The soft palate was intact and the posterior pharynx was normal, with no ulcerating or fungating growths. The remainder of the head and neck examination was unremarkable. Computed tomography (CT) scan showed extensive bony erosion of the nasal septum and hard palate, with mucosal thickening of the maxillary and ethmoid sinuses. There was no evidence of orbital or intracranial extension of this disease. Nasopharyngeal swab was positive for Staphylococcus aureus. Biopsy of the nasal cavity mucosa showed non-specific granulation tissue with no evidence of malignancy or infection.